Long Term Assessment of Adverse Cardiovascular Events in Men Receiving Androgen Deprivation Therapy Following Radical Prostatectomy
Skip to main content
eScholarship
Open Access Publications from the University of California

UC Irvine

UC Irvine Electronic Theses and Dissertations bannerUC Irvine

Long Term Assessment of Adverse Cardiovascular Events in Men Receiving Androgen Deprivation Therapy Following Radical Prostatectomy

Creative Commons 'BY' version 4.0 license
Abstract

Introduction: Androgen deprivation therapy (ADT) or radiation therapy (RT) with ADT is frequently recommended for biochemical recurrence (BCR) following a radical prostatectomy (RP). Probably the most severe life-threatening complication of ADT is an adverse cardiovascular event (ACE) such as acute myocardial infarction, stroke, etc. Because the literature is conflicted as to whether ADT increase ACEs. This study seeks to assess relationship of ACE in men undergoing ADT following RP.Methods: Retrospective review of prospectively collected data (n = 1895) from patients who underwent robot-assisted radical prostatectomy (RARP) performed by a single surgeon. 308 patients with a biochemical recurrence (BCR) and adequate follow-up data were analyzed for ACE. 189 men in the “treatment group” (TG) were managed with ADT or RT/ADT. The comparator group consisted of 119 men undergoing active observation (AO) with BCR but received no ADT or RT/ADT. Differences between AO and TG were analyzed utilizing student t-test and chi-squared (Table 1). Logistic regression was used to find predictors of ACE. Kaplan-Meier survival curves were generated to find time to ACE event and the percentage of patients that did not have an event. Results: At baseline, time of surgery, there was no significant difference in Charlson comorbidity index (CCI) but there was a trend in favor of AO (4.14 versus 4.38). In follow-up following BCR significant predictors of ACE in univariate analysis were age, CCI, body mass index (BMI), treatment status (AO vs TG), and smoking status (non-smoker vs previous smoker). 15-year Kaplan-Meier (KM) analysis showed a statistically significant increase in ACEs (TG 54.4% and AO 41.8%, p = 0.02). The driving factors for the increase in ACEs was coronary artery disease and arrhythmia. In the TG, there were no differences in ACE between ADT versus RT+ADT (55.4% versus 53.8%, p = 0.68). In adjusted multivariate logistic regression analysis, CCI and BMI were significant predictors for ACE with treatment status trending toward significance. Conclusions: There is an association between treatment for BCR and subsequent cardiovascular morbidity (as measured by ACE). Treatment may not undoubtedly cause ACE but that it may carry a higher risk of ACE. This effect may be attributed to time, or increasing the risk of particular types of ACE, but not to other types of ACE. We also saw the importance of BMI and CCI as a prognosticating tool for ACE, over treatment status.

Main Content
For improved accessibility of PDF content, download the file to your device.
Current View